The effects of alpha and beta-adrenergic stimulation on triacylglycerol secretion
were investigated in isolated rat hepatocytes. Epinephrine within 3h of incubation
suppressed triacylglycerol secretion by 35% and increased its cellular content
by 18%. The inhibitory effect of epinephrine was abolished by inclusion of
phentolamine and also prazosin but not with propranolol. Trifluoperazine concealed
the inhibitory effect of epinephrine in a dose-dependent manner, whereas
theobromine did not have any significant effect. The secretion of triacylglycerol
was suppressed not only by the a-agonist phenylephrine but also by the β-agonist
isoproterenol. Dibutyryl-cyclic AMP also inhibited secretion of triacylglycerol
by approximately 30%. The results indicate that epinephrine suppressed
triacylglycerol secretion via the α1-adrenoceptor whereas stimulation of beta-as
well as alpha-adrenoceptors can exert a similar effect. Calcium-calmodulin dependent
protein kinase may be involved in the down-regulation of VLDL secretion.
The unexpected effect of isoproterenol has been discussed in relation to
"dual signaling" and also the "store-dependent calcium entry" hypotheses.